Abstract
Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by repetitive behaviors, poor social skills, and difficulties with communication and hearing. The hearing deficits in ASD range from deafness to extreme sensitivity to routine environmental sounds. Previous research from our lab has shown drastic hypoplasia in the superior olivary complex (SOC) in both human cases of ASD and in an animal model of autism. However, in our study of the human SOC, we failed to find any changes in the total number of neurons in the ventral nucleus of the trapezoid body (VNTB) or any changes in cell body size or shape. Similarly, in animals prenatally exposed to the antiepileptic valproic acid (VPA), we failed to find any changes in the total number, size or shape of VNTB neurons. Based on these findings, we hypothesized that the neurotransmitter profiles, ascending and descending axonal projections of the VNTB are also preserved in these neurodevelopmental conditions. We investigated this hypothesis using a combination of immunohistochemistry and retrograde tract tracing. We found no difference between control and VPA-exposed animals in the number of VNTB neurons immunoreactive for choline acetyltransferase (ChAT). Additionally, we investigated the ascending projections from the VNTB to both the central nucleus of the inferior colliculus (CNIC) and medial geniculate (MG) and descending projections to the cochlea. Our results indicate no significant differences in the ascending and descending projections from the VNTB between control and VPA-exposed animals despite drastic changes in these projections from surrounding nuclei. These findings provide evidence that certain neuronal populations and circuits may be protected against the effects of neurodevelopmental disorders.
Highlights
The ventral nucleus of the trapezoid body (VNTB) is one of the periolivary nuclei within the superior olivary complex (SOC) – a multichannel processing station along the mammalian auditory pathway
Our initial observations that the VNTB was unaffected in these conditions was intriguing since VNTB neurons share a number of developmental features with other SOC nuclei, including origin, lineage and birthday (Altman and Bayer, 1980; Maricich et al, 2009; Marrs et al, 2013)
The majority of VNTB neurons are derived from rhombomeres 3 and 5 while MOC neurons are unique in the SOC in their origin from rhombomere 4 (Di Bonito et al, 2013; Marrs et al, 2013; Altieri et al, 2016)
Summary
The ventral nucleus of the trapezoid body (VNTB) is one of the periolivary nuclei within the superior olivary complex (SOC) – a multichannel processing station along the mammalian auditory pathway. VNTB neurons reside within the decussating axons of the trapezoid body that originate from neurons in the ventral cochlear nucleus (VCN) and are directed largely toward the SOC and nuclei of the lateral lemniscus. The VNTB includes about 4,500 neurons in rat (Kulesza et al, 2002) and 1,400 neurons in human (Kulesza, 2008). The VNTB includes a number of distinct neurochemical populations. During the early postnatal period VNTB neurons transition from using gamma amino butyric acid (GABA) to glycine as a neurotransmitter (Albrecht et al, 2014)
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